Autism gene’s loss hampers neurons’ trek through developing brain
Deleting an autism gene called TRIO derails neurons’ journey to their destination.
Deleting an autism gene called TRIO derails neurons’ journey to their destination.
Injecting cells called interneurons into the brains of a mouse model of autism restores typical social behavior. But the reason for this effect is a puzzle.
Mice missing a copy of CHD8, a top autism gene, show a signaling imbalance in their brains — a finding in line with a popular hypothesis about autism’s origins.
An experimental drug that muffles the activity of neurons in the skin moderates heightened reactions to touch in six mouse models of autism.
The signaling imbalance theory holds that the brains of autistic people are hyper-excitable because of either excess neuronal activity or weak brakes on that activity.
An analysis of four mouse models negates certain assumptions underlying the signaling imbalance theory of autism.
The brains of rats exposed in utero to the seizure drug valproate show a significant increase in brain size around the time of birth.
The largest genetic analysis of postmortem brain tissue to date has yielded maps of when and where genes related to autism are turned on and off throughout life.
Administering a cholesterol drug alongside an antibiotic eases atypical behavior and restores the signaling balance in the brains of people with fragile X syndrome.
Lattice-like structures that surround neurons may be overly abundant — or scarce — in brain regions of three autism mouse models.